Oxygen delivery, carbon dioxide removal, energy transfer to lungs and pulmonary hypertension behavior during venous-venous extracorporeal membrane oxygenation support: a mathematical modeling approach

Abstract

Objective To describe (1) the energy transfer from the ventilator to the lungs, (2) the match between venous-venous extracorporeal membrane oxygenation (ECMO) oxygen transfer and patient oxygen consumption (VO 2 ), (3) carbon dioxide removal with ECMO, and (4) the potential effect of systemic venous oxygenation on pulmonary artery pressure. Methods Mathematical modeling approach with hypothetical scenarios using computer simulation. Results The transition from protective ventilation to ultraprotective ventilation in a patient with severe acute respiratory distress syndrome and a static respiratory compliance of 20mL/cm H 2 O reduced the energy transfer from the ventilator to the lungs from 35.3 to 2.6 joules/minute. A hypothetical patient, hyperdynamic and slightly anemic with VO 2 = 200mL/minute, can reach an arterial oxygen saturation of 80%, while maintaining the match between the oxygen transfer by ECMO and the VO 2 of the patient. Carbon dioxide is easily removed, and normal PaCO 2 is easily reached. Venous blood oxygenation through the ECMO circuit may drive the PO 2 stimulus of pulmonary hypoxic vasoconstriction to normal values. Conclusion Ultraprotective ventilation largely reduces the energy transfer from the ventilator to the lungs. Severe hypoxemia on venous-venous-ECMO support may occur despite the matching between the oxygen transfer by ECMO and the VO 2 of the patient. The normal range of PaCO 2 is easy to reach. Venous-venous-ECMO support potentially relieves hypoxic pulmonary vasoconstriction.

Changes in haemodynamics during single lung transplantation under venovenous extracorporeal membrane oxygenation

“…HPV is maximal when mixed venous oxygen saturation (SvO 2 ) is normal and is decreased by either high or low SvO 2 [ 7 ]. The large elevation of SvO 2 during VV ECMO has been reported to potentially relieve HPV, reducing pulmonary pressure [ 8 ]. More importantly, hypercapnia is known to induce vasoconstriction of PA. Morimont et al [ 9 ] showed that veno-venous extracorporeal CO 2 removal reduced pulmonary vascular constriction related to hypercapnic acidosis and improved the pulmonary haemodynamics in a porcine acute respiratory distress syndrome model.…”

“…HPV is maximal when the mixed venous oxygen saturation (SvO 2 ) is normal and is decreased by either high or low SvO 2 [ 7 ]. A significant elevation of SvO 2 during VV ECMO was reported to potentially relieve HPV, reducing pulmonary pressure [ 8 ]. In addition, Morimont et al [ 9 ] reported that VV extracorporeal CO 2 removal ameliorated pulmonary hypertension (PH) and improved the right ventricular function in a porcine acute respiratory distress syndrome model.…”

Exploring the association of two oxygenators in parallel or in series during respiratory support using extracorporeal membrane oxygenation

“…We have previously described a multicompartmental mathematical model. ( 18 ) The background of oxygenation modeling was high-rated flow oxygenators. The rated flow of an oxygenator is defined by the amount of hypoxemic blood (oxygen saturation < 75%) that can be nearly fully saturated (95 - 100%) per minute.…”

The hemoglobin level impact on arterial oxygen saturation during venous-venous-extracorporeal membrane oxygenation support of acute respiratory distress syndrome patients: a mathematical marginal approach

“…( 5 ) We used a previously described mathematical marginal multicompartmental model of systemic SatO 2 during femoro-jugular VV-ECMO support. ( 6 ) This model accounts for recirculation proportional to ECMO blood flow and systemic, native lung and artificial lung compartments. To assess the effect of Hb level on systemic SatO 2 , we contrasted different scenarios related to patient and ECMO variables, such as systemic VO 2 rates, ECMO blood flow and CO, to highlight the dynamic care required by such patients.…”